Pathopharmacology, Immunity, Inflammation, and Cellular Regulation Practice Flashcards

Comprehensive practice flashcards covering Etiology, Pathogenesis, Pharmacokinetics, Pharmacodynamics, Immunology, Antibiotics, Cellular Injury, and Inflammatory Bowel Diseases from lecture notes.

What is the etiology of COVID-19?

COVID-19 is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which is a single-stranded RNA virus belonging to the coronavirus family.

Which receptor does SARS-CoV-2 target to facilitate entry into target cells?

The virus uses the angiotensin-converting enzyme 2 (ACE2) receptor, located in pneumocytes, myocardial cells, cholangiocytes, enterocytes, and oral mucosal epithelium.

What is the key difference in virulence and transmissibility between the COVID-19 Delta and Omicron variants?

The Delta variant is more virulent (causes very severe disease), whereas the Omicron variant is less virulent but more transmissible.

How do primary, secondary, and tertiary levels of prevention differ?

Primary prevention prevents disease from occurring by removing risk factors; secondary prevention detects and cures disease in the asymptomatic phase through early detection and treatment; tertiary prevention reduces complications of an established disease.

How does a diagnostic nasopharyngeal swab differ from an antibody blood test for COVID-19?

A nasopharyngeal swab detects the presence of the virus and indicates acute or current infection, whereas a blood test detects antibodies and does not indicate an acute or current infection.

What are the four phases of human clinical trials during drug evaluation?

Phase I tests chemicals on human volunteers; Phase II tests the drug on appropriate, informed patients; Phase III tests the drug in larger populations; Phase IV involves continual post-marketing evaluation.

What are the defining regulatory features of Schedule I (C-I) and Schedule V (C-V) controlled substances?

Schedule I drugs have high abuse potential and no accepted medical use (e.g., heroin, LSD). Schedule V drugs have limited abuse potential (e.g., codeine antidiarrheals) and limited quantities may be purchased without a prescription directly from a pharmacist by individuals at least $18\,\text{years}$ of age.

What is the first-pass effect in pharmacokinetics?

It is the process where orally administered medications are extensively metabolized by the liver before reaching systemic circulation. Alternative routes (such as IV, IM, sublingual, transdermal, and inhalational) avoid this effect.

Which enzyme is responsible for metabolizing approximately $25\%$ of common drugs in pharmacogenomics?

Cytochrome P450 2D6 (CYP2D6).

How do CYP450 enzyme inducers and inhibitors alter drug bioavailability?

Inducers increase drug metabolism, causing decreased bioavailability and risk of reduced therapeutic action. Inhibitors (such as grapefruit juice for CYP3A4) decrease drug metabolism, causing increased bioavailability and risk of adverse toxic effects.

How many half-lives are required for a drug to reach steady-state concentration in the body?

It requires at least $4$ to $5$ half-lives ($4$ half-lives achieve $93.8\%$ of steady-state; $5$ half-lives achieve $96.9\%$).

If $20\,\text{mg}$ of a medication with a half-life of $6\,\text{hours}$ is administered, how many milligrams remain in the body after $18\,\text{hours}$?

$2.5\,\text{mg}$ of the medication remains available, as $18\,\text{hours}$ equals $3$ half-lives ($20\,\text{mg} \rightarrow 10\,\text{mg} \rightarrow 5\,\text{mg} \rightarrow 2.5\,\text{mg}$).

What are the two patterns of reversible cellular injury?

1. Cellular swelling resulting from failure of the energy-dependent $Na^+/K^+$ ATPase membrane pump (hypoxic injury). 2. Fatty change linked to intracellular accumulation of fat.

What is the difference between homeostasis and allostasis?

Homeostasis aims to maintain a fixed steady state in response to physiological change, whereas allostasis maintains stability through change by anticipating needs and actively adjusting to predictable and unpredictable events.

What is the mechanism of action and clinical advantage of Celecoxib compared to Ibuprofen?

Celecoxib selectively inhibits the COX-2 enzyme required for prostaglandin synthesis without inhibiting COX-1, leading to reduced gastrointestinal (GI) adverse effects compared to non-selective NSAIDs like Ibuprofen.

Why must corticosteroid medications like Prednisone be tapered off gradually?

Prednisone suppresses normal adrenal function; stopping it abruptly can cause severe adrenal suppression.

What are the distinct functions of Helper T cells and Cytotoxic T cells in cell-mediated immunity?

Helper T cells assist other immune cells and present antigens to B cells for antibody production; Cytotoxic T cells detect and destroy cells infected with intracellular pathogens such as viruses.

Which immunoglobulin is the first to respond to acute infections?

IgM circulates in body fluids with five units to pull antigens together into clumps early during acute infections.

What severe adverse reactions and drug interactions are associated with Aminoglycosides like Gentamycin?

Ototoxicity and nephrotoxicity. Ototoxicity risk is increased when combined with loop diuretics.

What dietary and administration restrictions apply to Fluoroquinolones like Ciprofloxacin?

Ciprofloxacin should not be administered with calcium, magnesium, aluminum, iron, or zinc, and extended-release tablets must not be crushed, broken, or chewed.

What precautions and monitoring are required during IV administration of Vancomycin?

Monitor blood pressure throughout infusion, watch for 'red-man' syndrome, monitor hearing for ototoxicity, and check renal function (I&O, daily weight) and blood drug levels for nephrotoxicity.

What are the pathopharmacological differences between Crohn's Disease and Ulcerative Colitis?

Crohn's Disease features sharply demarcated, granulomatous 'cobblestone' skip lesions involving all layers of the bowel wall, primarily in the ileum. Ulcerative Colitis features continuous mucosal/submucosal ulcerative lesions starting in the rectum and left colon.

What are the key mechanisms and examples for Type I, Type II, Type III, and Type IV hypersensitivity reactions?

Type I: IgE-mediated activation of mast cells (e.g., anaphylaxis); Type II: IgG/IgM-mediated cytotoxic attack on cell surfaces (e.g., blood transfusion reaction); Type III: Antigen-antibody immune complex deposition in vessels (e.g., autoimmune vasculitis); Type IV: Sensitized T cell-mediated delayed tissue injury (e.g., positive PPD test).